Podcasts about lymphoid

The lymphatic system, or lymphoid system, is one of the components of the circulatory system, and it serves a critical role in both immune function and surplus extracellular fluid drainage.  Components of the lymphatic system include lymph, lymphatic vessels and plexuses, lymph nodes, lymphatic cells, and a variety of lymphoid organs. The pattern and form of lymphatic channels are more variable and complex but generally parallel those of the peripheral vascular system. The lymphatic system partly functions to convey lymphatic fluid, or lymph, through a network of lymphatic channels, filter lymphatic fluid through lymph nodes and return lymphatic fluid to the bloodstream, where it is eventually eliminated. Nearly all body organs, regions, and systems have lymphatic channels to collect the various byproducts that require elimination . Liver and intestinal lymphatics produce about 80% of the volume of lymph in the body. Notable territories of the body that do not appear to contain lymphatics include the bone marrow, epidermis, as well as other tissues where blood vessels are absent. The central nervous system was long considered to be absent of lymphatic vessels until they were recently identified in the cranial meninges. Moreover, a vessel appearing to have lymphatic features was also discovered in the eye. The lymphatic system is critical in a clinical context, particularly given that it is a major route for cancer metastasis and that the inflammation of lymphatic vessels and lymph nodes is an indicator of pathology.  Structure The lymphatic system includes numerous structural components, including lymphatic capillaries, afferent lymphatic vessels, lymph nodes, efferent lymphatic vessels, and various lymphoid organs.  Lymphatic capillaries are tiny, thin-walled vessels that originate blindly within the extracellular space of various tissues. Lymphatic capillaries tend to be larger in diameter than blood capillaries and are interspersed among them to enhance their ability to collect interstitial fluid efficiently. They are critical in the drainage of extracellular fluid and allow this fluid to enter the closed capillaries but not exit due to their unique morphology. Lymphatic capillaries at their blind ends are composed of a thin endothelium without a basement membrane. The endothelial cells at the closed end of the capillary overlap but shift to open the capillary end when interstitial fluid pressure is greater than intra-capillary pressure. This process permits lymphocytes, interstitial fluid, bacteria, cellular debris, plasma proteins, and other cells to enter the lymphatic capillaries. Special lymphatic capillaries called lacteals exist in the small intestine to contribute to the absorption of dietary fats. Lymphatics in the liver contribute to a specialized role in transporting hepatic proteins into the bloodstream. The lymphatic capillaries of the body form large networks of channels called lymphatic plexuses and converge to form larger lymphatic vessels. Lymphatic vessels convey lymph, or lymphatic fluid, through their channels. Afferent (toward) lymphatic vessels convey unfiltered lymphatic fluid from the body tissues to the lymph nodes, and efferent (away) lymphatic vessels convey filtered lymphatic fluid from lymph nodes to subsequent lymph nodes or into the venous system. The various efferent lymphatic vessels in the body eventually converge to form two major lymphatic channels: the right lymphatic duct and the thoracic duct.  The right lymphatic duct drains most of the right upper quadrant of the body, including the right upper trunk, right upper extremity, and right head and neck. The right lymphatic trunk is a visible channel in the right cervical region just anterior to the anterior scalene muscle. Its origin and termination are variable in morphology, typically forming as the convergence of the right bronchomediastinal, jugular, and subclavian trunks, extending 1 to 2 centimeters in length before returning its contents to the systemic circulation at the junction of the right internal jugular, subclavian, and/or brachiocephalic veins.  The thoracic duct, also known as the left lymphatic duct or van Hoorne's canal, is the largest of the body's lymphatic channels. It drains most of the body except for the territory of the right superior thorax, head, neck, and upper extremity served by the right lymphatic duct. The thoracic duct is a thin-walled tubular vessel measuring 2 to 6 mm in diameter. The length of the duct ranges from 36 to 45 cm. The thoracic duct is highly variable in form but typically arises in the abdomen at the superior aspect of the cisterna chyli, around the level of the twelfth thoracic vertebra (T12). The cisterna chyli, from which it extends, is an expanded lymphatic sac that forms at the convergence of the intestinal and lumbar lymphatic trunks extending along the L1-L2 vertebral levels. The cisterna chyli is present in approximately 40-60% of the population, and in its absence, the intestinal and lumbar lymphatic trunks communicate directly with the thoracic duct at the T12 level. As a result, the thoracic duct receives lymphatic fluid from the lumbar lymphatic trunks and chyle, composed of lymphatic fluid and emulsified fats, from the intestinal lymphatic trunk. Initially, the thoracic duct is located just to the right of the midline and posterior to the aorta. It exits the abdomen and enters the thorax via the aortic hiatus formed by the right and left crura of the diaphragm, side by side with the aorta. The thoracic duct then ascends in the thoracic cavity just anterior and to the right of the vertebral column between the aorta and azygos vein. At about the level of the fifth thoracic vertebra (T5), the thoracic duct typically crosses to the left of the vertebral column and posterior to the esophagus. From here, it ascends vertically and usually empties its contents into the junction of the left subclavian and left internal jugular veins in the cervical region. To ensure that lymph does not flow backward, collecting lymphatic vessels and larger lymphatic vessels have one-way valves. These valves are not present in the lymphatic capillaries. These lymphatic valves permit the continued advancement of lymph through the lymphatic vessels aided by a pressure gradient created by vascular smooth muscle, skeletal muscle contraction, and respiratory movements. However, it is important to note that lymphatic vessels also communicate with the venous system through various anastomoses. Lymph nodes are small bean-shaped tissues situated along lymphatic vessels. Lymph nodes receive lymphatic fluid from afferent lymphatic vessels and convey lymph away through efferent lymphatic vessels. Lymph nodes serve as a filter and function to monitor lymphatic fluid/blood composition, drain excess tissue fluid and leaked plasma proteins, engulf pathogens, augment an immune response, and eradicate infection. Several organs in the body are considered to be lymphoid or lymphatic organs, given their role in the production of lymphocytes. These include the bone marrow, spleen, thymus, tonsils, lymph nodes, and other tissues. Lymphoid organs can be categorized as primary or secondary lymphoid organs. Primary lymphoid organs are those that produce lymphocytes, such as the bone marrow and thymus. Bone marrow is the primary site for the production of lymphocytes. The thymus is a glandular organ located anterior to the pericardium. It serves to mature and develop T cells, or thymus cell lymphocytes, in response to an inflammatory process or pathology. As individuals age, both their bone marrow and thymus reduce and accumulate fat. Secondary lymphoid organs serve as territories in which immune cells function and include the spleen, tonsils, lymph nodes, and various mucous membranes, such as in the intestines. The spleen is a purplish, fist-sized organ in the left upper abdominal quadrant that contributes to immune function by serving as a blood filter, storing lymphocytes within its white pulp, and being a site for an adaptive immune response to antigens. The lingual tonsils, palatine tonsils, and pharyngeal tonsils, or adenoids, work to prevent pathogens from entering the body. Mucous membranes in the gastrointestinal, respiratory, and genitourinary systems also function to prevent pathogens from entering the body. Lymph Lymphatic fluid, or lymph, is similar to blood plasma and tends to be watery, transparent, and yellowish in appearance. Extracellular fluid leaks out of the blood capillary walls because of pressure exerted by the heart or osmotic pressure at the cellular level. As the interstitial fluid accumulates, it is picked up by the tiny lymphatic capillaries along with other substances to form lymph. This fluid then passes through the lymphatic vessels and lymph nodes and finally enters the venous circulation. As the lymph passes through the lymph nodes, both monocytes and lymphocytes enter it.  Lymph is composed primarily of interstitial fluid with variable amounts of lymphocytes, bacteria, cellular debris, plasma proteins, and other cells. In the GI tract, lymphatic fluid is called chyle and has a milk-like appearance that is chiefly due to the presence of cholesterol, glycerol, fatty acids, and other fat products. The vessels that transport the lymphatic fluid from the GI tract are known as lacteals. Embryology The development of the lymphatic system is known from both human and animal, especially mouse studies. The lymphatic vessels form after the development of blood vessels, around six weeks post-fertilization. The endothelial cells that serve as precursors to the lymphatics arise from the embryonic cardinal veins. The process by which lymphatic vessels form is similar to that of the blood vessels and produces lymphatic-venous and intra-lymphatic anastomoses, but diverse origins exist for components of lymphatic vessel formation in different regions.  Six primary lymph sacs develop and are apparent about eight weeks post-fertilization. These include, from caudal to cranial, one cisterna chyli, one retroperitoneal lymph sac, two iliac lymph sacs, and two jugular lymph sacs. The jugular lymph sacs are the first to develop, initially appearing next to the jugular part of the cardinal vein. Lymphatic vessels then form adjacent to the blood vessels and connect the various lymph sacs. The lymphatic vessels primarily arise from the lymph sacs through the process of self-proliferation and polarized sprouting.  Stem/progenitor cells play a huge role in forming lymphatic tissues and vessels by contributing to sustained growth and postnatally differentiating into lymphatic endothelial cells. Lymphatic channels from the developing gut connect with the retroperitoneal lymph sac and the cisterna chyli, situated just posteriorly. The lymphatic channels of the lower extremities and inferior trunk communicate with the iliac lymph sacs. Finally, lymphatic channels in the head, neck and upper extremities drain to the jugular lymph sacs. Additionally, a right and left thoracic duct form and connect the cisterna chyli with the jugular lymph sacs and form anastomoses that eventually produce the typical adult form. The lymph sacs then produce groups of lymph nodes in the fetal period. Migrating mesenchyme enters the lymph sacs and produces lymphatic networks, connective tissue, and other layers of the lymph nodes. Function The lymphatic system's primary function is to balance the volume of interstitial fluid and convey it and excess protein molecules into the venous circulation. The lymphatic system is also important in immune surveillance, defending the body against foreign particles and microorganisms. It does so by conveying antigens and leukocytes to lymph nodes, where antigen-primed and targeted lymphocytes and other immune cells are conveyed into the lymphatic vessels and blood vessels. In addition, the system has a role in the absorption of fat-soluble vitamins and fatty substances in the gut via the gastrointestinal tract's lacteals within the villi and the transport of this material into the venous circulation.  Newly recognized lymphatic vessels are visible in the meninges relating to cerebrospinal fluid (CSF) outflow from the central nervous system. Finally, lymphatics may play a role in the clearance of ocular fluid via the lymphatic-like Schlemm canals. Clinical Significance Leaks of lymphatic fluid occur when the lymphatic vessels are damaged. In the abdomen, lymphatic vessel damage may occur during surgery, especially during retroperitoneal procedures such as repairing an abdominal aortic aneurysm. These leaks tend to be mild, and the vessels in the peritoneum and mesentery eventually absorb the lymphatic fluid or chyle. However, when the thoracic duct is injured in the chest, the chyle leak can be extensive. In most cases, conservative care with a no-fat diet (medium chain triglycerides) or total parenteral nutrition is unsuccessful. In most cases, if the injury to the thoracic duct was surgical, a surgical procedure is required to tie off the duct. If the thoracic duct is injured in the cervical region, then inserting a drainage tube and adopting a low-fat diet will help seal the leak. However, thoracic duct injury in the chest cavity usually requires drainage and surgery. It is rare for the thoracic segment of the thoracic duct to seal on its own. In terms of accumulation of chyle in the thorax (i.e., chylothorax), if a patient has an injury to the thoracic duct in the thorax below the T5 vertebral level, then fluid will collect in only the right pleural cavity. If the injury is to the thoracic duct in the thorax above the T5 vertebral level, then fluid will appear in both pleural cavities.   Other Issues The lymphatic system is prone to disorders like the venous and arterial circulatory systems. Developmental or functional defects of the lymphatic system cause lymphedema. When this occurs, the lymphatic system is unable to sufficiently drain lymphatic fluid resulting in its accumulation and swelling of the territory. Lymphedema, this swelling due to the accumulation of lymph, is classified as primary or secondary. Primary lymphedema is an inherited disorder where the lymphatic system development has been disrupted, causing absent or malformed lymphatic tissues. This condition often presents soon after birth, but some conditions may present later in life (e.g., at puberty or later adulthood). There are no effective treatments for primary lymphedema. Past surgical treatments were found to be mutilating and are no longer implemented. The present-day treatment revolves around compression stockings, pumps, and constrictive garments. Secondary lymphedema is an acquired disorder involving lymphatic system dysfunction that may result from many causes, including cancer, infection, trauma, or surgery. The treatment of secondary lymphedema depends on the cause. Oncological and other surgeries may result in secondary lymphedema due to the removal or biopsy of lymph nodes or lymphatic vessels. Non-surgical lymphedema may result from malignancies, obstruction within the lymphatic system, infection, or deep vein thrombosis. In most cases of obstructive secondary lymphedema, the drainage will resume if the inciting cause is removed, although some individuals may need to wear compressive stockings permanently. Also, physical therapy may help alleviate lymphedema when the extremities are involved. There is no absolute cure for lymphedema, but diagnosis and careful management can help to minimize complications. Lymphomas are cancers that arise from the cells of the lymphatic system. There are numerous types of lymphoma, but they are grouped into Hodgkin lymphoma and non-Hodgkin lymphoma. Lymphomas usually arise from the malignant transformation of specific lymphocytes in the lymphatic vessels or lymph nodes in the gastrointestinal tract, neck, axilla, or groin. Symptoms of lymphoma may include night sweats, fever, fatigue, itching, and weight loss. Cancers originating outside of the lymphatic system often spread via the lymphatic vessels and may involve regional lymph nodes serving the impacted organs or tissues. Lymphadenitis occurs when the lymph nodes become inflamed or enlarged. The cause is usually an adjacent bacterial infection but may also involve viruses or fungi. The lymph nodes usually enlarge and become tender. Lymphatic filariasis, or elephantiasis, is a very common mosquito-borne disorder caused by a parasite found in tropical and subtropical areas of the world, including Africa, Asia, the Pacific, the Caribbean, and South America. This condition involves parasitic microscopic nematodes (roundworms) that infect the lymphatic system and rapidly multiply and disrupt lymphatic function. Many infected individuals may have no outward symptoms, although the kidneys and lymphatic tissues may be damaged and dysfunctional. Symptomatic individuals may present with disfigurement caused by significant lymphedema and elephantiasis (thickening of the skin, particularly the extremities). The parasite may also cause hydrocele, an enlargement of the scrotum due to the accumulation of fluid, which may result from obstruction of the lymph nodes or vessels in the groin. Individuals presenting with symptoms have poorly draining lymphatics, often involving the extremities, resulting in huge extremities and marked disability. Lymphatic filariasis is the most common cause of disfigurement in the world, and it is the second most common cause of long-term disability.  (credits: NIH)

In this episode, we review the high-yield topic of⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Primary Lymphoid Tissue ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Immunology section.Follow⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets

Drs. Sanam Loghavi and Amer Zeidan delve into the history behind the recent classification split between the World Health Organization (WHO) and the International Consensus Classification (ICC) for myeloid and lymphoid malignancies, and how a few years of minor disagreement have culminated in a unified system. They explore the critical differences in how myeloid and lymphoid neoplasms are now categorized, what this alignment means for pathologists, oncologists, regulators, and patients, when the new classification will take effect, and how it is expected to influence research, diagnosis, and clinical care. Check out Chadi's website for all Healthcare Unfiltered episodes and other content. www.chadinabhan.com/ Watch all Healthcare Unfiltered episodes on YouTube. www.youtube.com/channel/UCjiJPTpIJdIiukcq0UaMFsA

Send us a textLeveraging AI for Deep Insights into Tertiary Lymphoid Structures in Colorectal CancerIn this episode of the Digital Pathology Podcast, I introduce 'Aleks + AI,' a new experimental series leveraging Google's Notebook LM to delve deeper into scientific literature. Today's focus is on tertiary lymphoid structures (TLS) and their potential to predict colorectal cancer prognosis. We discuss a study published in the October 2024 issue of Precision Clinical Medicine, exploring different methods of quantifying TLS using digital pathology and AI.  The paper title is: "Comparative analysis of tertiary lymphoid structures for predicting survival of colorectal cancer: a whole-slide images-based study"The findings highlight TLS density as a reliable predictor of survival and its correlation with immune responses and microsatellite instability. We also touch upon the potential for AI to streamline TLS analysis in clinical settings and the broader implications for personalized medicine. Join us as we dive into the intersection of digital pathology and computer science, featuring insights and commentary from my AI co-hosts, Hema and Toxy.00:00 Welcome and Introduction00:45 Introducing the New AI Tool: Notebook LM by Google01:11 Experimental Series: "Aleks + AI"02:06 Deep Dive into Tertiary Lymphoid Structures (TLS)03:18 Understanding TLS and Their Role in Colorectal Cancer04:20 Quantification Methods and Key Findings05:02 Implications for Personalized Medicine09:02 AI in TLS Analysis and Future Prospects11:00 CMS Classification and TLS Density12:08 Study Limitations and Future Directions15:40 Final Thoughts and Wrap-Up16:28 Feedback and Future PlansTHIS EPISODE'S RESOURCES116: DigiPath Digest #18 | Federated Learning in Pathology. Developing AI Models While Preserving PrivacyPUBLICATION DISCUSSED TODAY

In this episode, we review the high-yield topic of⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Secondary Lymphoid Tissue⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Immunology section. Follow ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

Dupi and CTCL... It's complicated - Dupi and lymphoid reactions - Dupi worsens CTCL - Updates in CSU pathophys and treatment - Calcinosis cutis options - Petroleum jelly: It's awesome, and here's why - Want to donate to the cause? Do so here! Donate to the podcast: uofuhealth.org/dermasphere Check out our video content on YouTube: https://www.youtube.com/@dermaspherepodcast and VuMedi!: https://www.vumedi.com/channel/dermasphere/ The University of Utah's Dermatology ECHO: ⁠https://physicians.utah.edu/echo/dermatology-primarycare - ⁠ Connect with us! - Web: ⁠https://dermaspherepodcast.com/⁠ - Twitter: @DermaspherePC - Instagram: dermaspherepodcast - Facebook: https://www.facebook.com/DermaspherePodcast/ - Check out Luke and Michelle's other podcast, SkinCast! ⁠https://healthcare.utah.edu/dermatology/skincast/⁠ Luke and Michelle report no significant conflicts of interest… BUT check out our friends at: - ⁠Kikoxp.com ⁠(a social platform for doctors to share knowledge) - ⁠https://www.levelex.com/games/top-derm⁠ (A free dermatology game to learn more dermatology!)

Reference Cancer Discov. 2022 Mar 1; 12(3): 856–871. --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

References Nat Protoc. 2017 Nov;12(11):2342-2354 Annual Review of Immunology 2021. Volume 39. pp 279-311 Immunity 2022. Volume 55, Issue 8. Pages 1402-1413.e4 --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

References Immunity 2022. 55, Issue 8. Pages 1402-1413. Methods Mol Biol. 2018;1675:167-181. Experimental & Molecular Medicine 2019. volume 51, Article number: 80. Cell Reports 2015 10, 2043-2054DOI: (10.1016/j.celrep.2015.02.057) --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

Before we're even born, our bodies begin to grow and train an army of spies and assassins, creating a crew of immune system fighters in the upper chest's thymus gland. While this production is dominated by T cells, other immune cells such as B cells and plasma cells can be generated within the thymus, albeit at a very low level.   After adolescence, the thymus reduces production at its 'spy and assassin' factory to a trickle. This has consequences because as we age, our immune system makes mistakes, leading to mutations in our DNA; changes in the types of antibodies we produce, and odd feedback loops.   Those glitches contribute to the generation of chronic lymphocytic leukemia or B-cell lymphomas such as non-Hodgkin lymphoma. They can also contribute to the development of autoimmune diseases such as lupus and myasthenia gravis.   "We think this all has to do with a life-or-death signalling loop," said Dr. Peter Pioli, who moved to the University of Saskatchewan last year to become an assistant professor of Biochemistry, Microbiology & Immunology. In February, he published his findings in iScience.   "For autoimmune patients, you get this thymus that gets filled up with all these B-cells and plasma cells, so you no longer have this little trickle; you have a bit of a runaway train," he said.   Using mouse models, Pioli and his team are trying to piece together the triggers convincing aging B-cells to mistakenly ramp up plasma cell production. They want to know how this impacts the development of various diseases.   In this episode, Pioli explains his interest in plasma cells.   "It  fascinates and confounds you all in one," said Pioli. "This one cell has to have this perfectly aligned machinery to do this. And it's kind of hard to look away when you find something like that."   A "curious troublemaker" who loved to tinker as a kid, Pioli remembers taking apart tools and objects in his parents' garage, removing pieces and trying to rebuild them. That curiosity carried him through his undergraduate, graduate studies and post-doctoral work in Wisconsin, Utah, and California.   "It's just a lot of fun," said Pioli. "You get the payoff of hopefully finding something that could actually help someone someday: understanding aging, understanding these breakdowns that lead to autoimmune diseases and tissue breakdown."   Pioli admits his scientific career has taken plenty of detours, but he's extremely grateful it unfolded the way it did.   "There's a lot you learn from that, not just in terms of experience," he said. "You also learn about yourself in terms of your potential to persevere.  And maybe the potential to be supremely stubborn, to keep at it."

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.17.537109v1?rss=1 Authors: Meza Guzman, L. G., Hyland, C. D., Bidgood, G. M., Leong, E., Shen, Z., Goh, W., Kratina, T., Rautela, J., Vince, J., Nicholson, S., Huntington, N. Abstract: The clinical development of Natural Killer (NK) cell-mediated immunotherapy marks a milestone in the development of new cancer therapies and has gained traction due to the intrinsic ability of the NK cell to target and kill tumour cells. To fully harness the tumour killing ability of NK cells, we need to improve NK cell persistence and overcome suppression of NK cell activation in the tumour microenvironment. The trans-membrane, protein tyrosine phosphatase CD45, regulates NK cell homeostasis, with genetic loss of CD45 in mice resulting in increased numbers of mature NK cells [1-3]. This suggests that CD45-deficient NK cells might display enhanced persistence following adoptive transfer. However, here we demonstrated that adoptive transfer of CD45-deficiency did not enhance NK cell persistence in mice, and instead, the homeostatic disturbance of NK cells in CD45-deficient mice stemmed from a developmental defect in the common lymphoid progenitor population. The enhanced maturation within the CD45-deficient NK cell compartment was intrinsic to the NK cell lineage, and independent of the developmental defect. CD45 is not a conventional immune checkpoint candidate, as systemic loss is detrimental to T and B cell development [4-6], compromising the adaptive immune system. Nonetheless, this study suggests that inhibition of CD45 in progenitor or stem cell populations may improve the yield of in vitro generated NK cells for adoptive therapy. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.16.532850v1?rss=1 Authors: Barron, J. J., Mroz, N. M., Taloma, S. E., Dahlgren, M. W., Ortiz-Carpena, J. F., Dorman, L. C., Vainchtein, I. D., Escoubas, C. C., Molofsky, A. B., Molofsky, A. V. Abstract: The innate immune system plays essential roles in brain synaptic development, and immune dysregulation is implicated in neurodevelopmental diseases. Here we show that a subset of innate lymphocytes (group 2 innate lymphoid cells, ILC2s) is required for cortical inhibitory synapse maturation and adult social behavior. ILC2s expanded in the developing meninges and produced a surge of their canonical cytokine Interleukin-13 (IL-13) between postnatal days 5-15. Loss of ILC2s decreased cortical inhibitory synapse numbers in the postnatal period where as ILC2 transplant was sufficient to increase inhibitory synapse numbers. Deletion of the IL-4/IL-13 receptor (Il4ra) from inhibitory neurons phenocopied the reduction inhibitory synapses. Both ILC2 deficient and neuronal Il4ra deficient animals had similar and selective impairments in adult social behavior. These data define a type 2 immune circuit in early life that shapes adult brain function. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this week's episode we'll discuss the benefits of early diagnosis and hematopoietic stem cell transplant in patients with hypomorphic RAG deficiency, learn more about EBV-driven lymphoid neoplasms associated with pediatric ALL maintenance therapy, and analyze the associations between clonal hematopoiesis and recurrent vascular events and death in patients with ischemic stroke. 

Our lab studies immune dysfunction within the female gynecological disease of endometriosis. My specific project is looking at the relationship between a protein called interleukin 33, or IL-33, and a type of immune cell known as group 2 innate lymphoid cells, and how their contributing to disease severity and symptomology. For upcoming interviews check out […]

Listen to a soundcast of the 8/24/22 and 8/26/22 FDA approvals of Imbruvica (ibrutinib) for pediatric patients with chronic graft versus host disease, including a new oral suspension, and Pemazyre (pemigatinib) for relapsed or refractory myeloid/lymphoid neoplasms with FGFR1 rearrangement.”

Dr Verstovsek discusses the FDA approval of pemigatinib in myeloid/lymphoid neoplasms with FGFR1 rearrangements, the transformative effects of pemigatinib, and the importance of identifying chromosomal abnormalities in patients with this aggressive disease.

In this episode, we review the high-yield topic of Primary Lymphoid Tissue from the Immunology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficialx Twitter: www.twitter.com/medbulletsIn this episode --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

In this podcast, Dr. Truchetet discusses her work on the role of innate lymphoid cells in the fibrotic processes in systemic sclerosis (SSc) patients. The group of Dr. Truchetet found that ILC2 are crucial mediators of skin fibrosis in SSc and that combined treatment of patients with TGFb inhibitors and IL-10 might be an attractive new therapeutic approach in SSc. Read the full paper on the ARD website: https://ard.bmj.com/content/80/12/1594 Please subscribe to the ARD podcast on all podcast platforms, including Apple Podcast, Google Podcasts, Stitcher and Spotify. If you enjoy the show, feel free to leave us a comment or a review on the podcast iTunes page (https://podcasts.apple.com/gb/podcast/ard-podcast/id1171058059).

This is the eighth of a series of short videos on Low dose Medicine and in particular Cytokines. This video introduces the cytokine Interleukin 7. More information about this and other health topics can be found in my books "Low Dose Medicine" and "Cure Without Side effects" by following these links: ►►►https://amzn.to/3Bbx8fd ►►►https://amzn.to/36iaqDU To check the Low dose Medicine health kit follow this link: ►►►https://kit.co/cureswithoutsideffect/low-dose-medicine DISCLAIMER: Nothing contained in this video is intended nor can be taken to diagnose, treat, or cure any disease. It is for informational purposes only. --- Send in a voice message: https://anchor.fm/cureswithoutsideeffects/message

ILC3 can contribute to the progression and aggravation of IBD's while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR− ILC3 or NCR+ ILC3 function NCR (natural cytotoxicity receptors), are type 1 transmembrane proteins of the immunoglobulin superfamily. Upon stimulation, NCR's mediate NK killing and release of IFNγ. They bind viral ligands such as hemagglutinins, neuraminidases, bacterial ligands, and cellular ligands related with auto immune diseases, tumour growth, and associated aging morbidity. References Experimental & Molecular Medicine volume 51, Article number: 80 (2019) Cell Death & Disease volume 10, Article number: 315 (2019) Front. Immunol., 28 September 2015 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Commentary by Dr. Valentin Fuster

In this episode, we review the high-yield topic of Secondary Lymphoid Tissue from the Immunology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Dr. Pagel discusses the advances that have been made with PI3K inhibitors in lymphoid malignancies, the impact of the FDA approval of umbralisib on the treatment paradigm in follicular lymphoma and marginal zone lymphoma, and ongoing research poised to expand the armamentarium.

FA 2020 - p96 lymphoid structures

Talk to a Dr. Berg Keto Consultant today and get the help you need on your journey (free consultation). Call 1-540-299-1557 with your questions about Keto, Intermittent Fasting, or the use of Dr. Berg products. Consultants are available Monday through Friday from 8 AM to 10 PM EST. Saturday & Sunday from 9 AM to 6 PM EST. USA Only. Take Dr. Berg's Free Keto Mini-Course! In this podcast, we're going to talk about how stress affects your health. Chronic stress can literally destroy your immune system. Cortisol is activated by stress. Lymphoid tissue is an area where you have a lot of immune reactions to keep pathogens away from different organs. High cortisol will divert amino acids from the lymphoid tissue, basically shrinking this tissue. It makes your immune system smaller. Antibodies are produced by the immune system, and they help develop immunity. They don't necessarily kill pathogens, but they put a tag on them for other immune cells to kill them. If you have enough antibodies in your system, you are protected. But, with high cortisol, you can have a decrease in overall antibody production. You also have various barriers of immune defense. But, high cortisol can create a break down in your cellular barriers, which can raise your susceptibility to viral and bacterial infections. Keeping your immune system strong isn't just about good nutrition; it's also about keeping your stress as low as possible. Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional & natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government & the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning. FACEBOOK: fb.me/DrEricBerg?utm_source=Podcast&utm_medium=Anchor TWITTER: http://twitter.com/DrBergDC?utm_source=Podcast&utm_medium=Post&utm_campaign=Daily%20Post YOUTUBE: http://www.youtube.com/user/drericberg123?utm_source=Podcast&utm_medium=Anchor DR. BERG'S SHOP: https://shop.drberg.com/?utm_source=Podcast&utm_medium=Anchor MESSENGER: https://www.messenger.com/t/drericberg?utm_source=Podcast&utm_medium=Anchor DR. BERG'S VIDEO BLOG: https://www.drberg.com/blog?utm_source=Podcast&utm_medium=Anchor

This episode covers the Immunology chapter of Crush Step 1, including topics such as:- Lymphoid structures- Innate versus adaptive immunity- Cells of the immune system- Major Histocompatibility Complex 1 & 2 - B cells, antibodies, and humoral immunity- T cells, cell-mediated immunity, and immune system regulation- Complement system- Hypersensitivity response- Transplantation immunologyGet a discount on best selling study resources from Elsevier ITB listeners can get 30% off of books like Crush Step 1, USMLE Step 2 Secrets, Netter’s Anatomy Coloring Book, and more! Head over to us.elsevierhealth.com/insidetheboards and use the code ITB30 at checkout.About the Crush Step 1 Podcast With a focus on teaching you to “think like a question writer”, InsideTheBoards is the leading producer of medical education podcasts. The Crush Step 1 podcast, the second collaboration between InsideTheBoards and Elsevier, features a totally free, audio optimized, complete narration of Crush Step 1: The Ultimate USMLE Step 1 Review by Ted O'Connell, Ryan Pedigo, and Thomas Blair. Crush Step 1 features up-to-date, easy-to-read (or listen to), high yield info on all the material tested on the exam with topics selected by a review board of current medical students and residents who scored in the 99th percentile on the USMLE Step 1. The Crush Step 1 podcast is the perfect companion for your dedicated prep time. InsideTheBoards Study Smarter Podcast Each year during the dedicated prep time we run a “Study Smarter Series for the USMLE Step 1 and COMLEX Level 1” on our Study Smarter Podcast with a focus exclusively on breaking down USMLE style questions. Click here to check it out on iTunes or visit our BRAND NEW Website ITB Audio Qbank and iOS Beta AppThe Audio Qbank by InsideTheBoards mobile app has both free and premium features and is available on both Android and iOS. To get started, first, create a Boardsinsider Account on our website insidetheboards.comFree Features All of our podcasts in one place organized into playlists for easy studying (also with less ads and exclusive content) Mindfulness meditations designed specifically for medical students A monthly offering of high yield content (questions dissections, audio qbank samples) available only on our mobile app. Early Access and exclusive content like a preview of the soon to be released "Crush Step 1" podcast and the "Inside ITB" podcast where we "get real" about the challenges of building ITB and the day to day behind the scenes stuff. Premium FeaturesSubscribe to an ITB premium account and get additional features Access to 500+ audio optimized board style practice questions in our Audio Qbank. The Step 1 version is powered by Exam Circle and the Step 2 Version is powered by OnlineMedEd. New questions added each month. High Yield Pharmacology (powered by Lecturio) with 100 of the top pharm questions you need to know for both Step 1 and Step 2 Audio Flashcards (coming soon) Our audio qbank is PERFECT for studying for the boards on the go. And we're adding content and improving it all the time. Learn more about the Audio Qbank by InsideTheBoards mobile app hereInsideTheBoards, Elsevier and their collaborators are not affiliated with the NBME, USMLE, COMLEX, NBOME or any professional licensing body. InsideTheBoards and its partners fully adhere to the policies on irregular conduct outlined by the aforementioned credentialing bodies.

Some cancers come for dogs right away, and others take longer. Chronic Lymphocytic Leukemia (CLL) can be hard to diagnose, because it often develops while the dog acts totally healthy. But routine blood tests can tip a veterinarian off that something is wrong … and when you know early there are lots of things you can do to help your dog. Today James Jacobson takes a question about CLL, also known as Lymphoid Leukemia, from Delisa in Alabama, and asks Dr. Dressler for an answer. Dr. Demian Dressler is co-author of our podcast sponsor, the book The Dog Cancer Survival Guide: Full Spectrum Treatments to Optimize Your Dog’s Life Quality and Longevity.  Links Mentioned in Today’s Show:  The Dog Cancer Survival Guide: Full Spectrum Treatments to Optimize Your Dog’s Life Quality and Longevity. Apocaps can be found in many veterinary offices and online, including at https://Apocaps.comK9 Immunity can be found in many places online, including at https://www.k9medicinals.comDelisa is a member of the private Facebook group for readers of Dr. Dressler’s book “The Dog Cancer Survival Guide” https://www.facebook.com/groups/dogcancersupport/  Here’s a good article on lymphoid leukemia or lymphocytic leukemia on the National Canine Cancer Foundation’s website: https://wearethecure.org/learn-more-about-canine-cancer/canine-cancer-library/lymphoid-leukemia/Here’s a good article that will help you to understand the difference among blood cancers, including chronic lymphocytic leukemia: https://www.vetfolio.com/learn/article/lymphoid-leukemia-in-dogsYou can reach out to Dr. Demian Dressler directly on his veterinary hospital’s website: https://VetinKihei.com.   Quick Overview of CLL from James Jacobson’s conversation with Dr. Nancy Reese:First, let’s get clarity on this disease a little, because it’s often confused with a much more common dog cancer called lymphoma. To find out more, I asked one of our Full Spectrum veterinarians, Dr. Nancy Reese about Chronic Lymphocytic Leukemia, also known as Chronic Lymphoid Leukemia, or CLL for short. I don’t have tape of our conversation about CLL, but you’ll hear from Dr. Nancy in an upcoming episode about Covid-19.By email, Dr. Nancy explained that lymphoma and lymphocytic leukemia are both cancers of the lymphocytes. What’s a lymphocyte? It’s a type of white blood cell that is born in the bone marrow, and less often, the spleen. Those white blood cells circulate in the blood stream and the lymph system, fighting infections in cells all over the body. So, when lymphocytes get cancer, you’ve got a systemic disease, which means the cancer is everywhere by definition. In lymphoma, the cancerous lymphocytes tend to collect in the lymph glands, which tend to get swollen. In lymphocytic leukemia, the cancerous lymphocytes tend to circulate in the bloodstream. Same cells, different locations in the body. Either way, the cancer cells, the lymphoid or lymphocytic cells, are everywhere ... so when you get this diagnosis, the veterinarian will almost always recommend chemotherapy. That's the only conventional treatment that circulates in the blood and goes everywhere in the body, right?So today’s question is this: when do you need to start the chemo for Lymphoid or Lymphocytic Leukemia? Right when you get the diagnosis? Or can you wait a while?Well, the answer depends on whether the lymphocytic leukemia is acute or chronic!Chronic conditions are long-developing, as opposed to severe and sudden, or acute conditions. Right? So Chronic Lymphocytic Leukemia is a long-developing cancer of lymphocytes. Also, Dr. Nancy added, the lymphocytes involved in CLL are mature and divide slowly, at the same rate as a normal cell. So that’s one reason this form of the cancer takes a long time to develop.There is an acute form of lymphocytic leukemia, as well, that is much more immediately dangerous, and it develops in a immature form of the lymphocyte cells, a form that rapidly divides. So the Acute Lymphocytic Leukemia, or ALL, divides very fast, comes on suddenly, and rapidly progresses.We’ll hear more from Dr. Nancy directly in an upcoming episode about coronavirus and dogs that is literally a must-listen. She’s the perfect person to ask about the pandemic we’re in right now, because she is not only a veterinarian with thirty years of experience under her belt, she’s also got a Ph.D. in Epidemiology.About Today’s Guest, Dr. Demian Dressler:  Dr. Demian Dressler, DVM is internationally recognized as “the dog cancer vet” because of his innovations in the field of dog cancer management. A dynamic educator and speaker, Dr. Dressler is the author of the best-selling animal health book The Dog Cancer Survival Guide: Full Spectrum Treatments to Optimize Your Dog’s Life Quality and Longevity.  Dr. Dressler is the owner of the accredited practice South Shore Veterinary Care, a full-service veterinary hospital in Maui, Hawaii, Dr. Dressler studied Animal Physiology and received a Bachelor of Science degree from the University of California at Davis before earning his Doctorate in Veterinary Medicine from Cornell University.  "Your dog does NOT have an expiration date, and there are things ALL cancers have in common that you can help fight. Imagine looking back at this time five years from now and not having a single regret."  - Dr. DYou can find hundreds of articles Dr. D wrote about dog cancer on his immensely popular website: https://www.dogcancerblog.com/meet-the-veterinarians-dr-dressler/  Follow Dr. D and The Dog Cancer Survival Guide on the Socials:    https://www.youtube.com/dogcancervet  https://www.facebook.com/dogcancer/  https://www.facebook.com/groups/dogcancersupport/  https://twitter.com/dogcancervet  https://www.instagram.com/dogcancersurvivalguide/   Dog Cancer Answers is a Maui Media production in association with Dog Podcast NetworkThis episode is sponsored by the best-selling animal health book The Dog Cancer Survival Guide: Full Spectrum Treatments to Optimize Your Dog’s Life Quality and Longevity by Dr. Demian Dressler and Dr. Susan Ettinger. Available everywhere fine books are sold. Listen to podcast episode for a special discount code. If you would like to ask a dog cancer related question for one of our expert veterinarians to answer on a future Q&A episode, call our Listener Line at 808-868-3200.Have a guest you think would be great for our show? Contact our producers at DogCancerAnswers.comHave an inspiring True Tail about your own dog’s cancer journey you think would help other dog lovers? Share your true tail with our producers.

Tumor Lysis Syndrome + MCQ from chapter titled Emergencies in Hematology and Oncology in Baliga's Textbook of Internal Medicine available at MasterMedFacts.com authored by Thorvardur Halfdanarson,MD Professor of Oncology Mayo Clinic, Rochester, MN & Eric Engelman, MD Clinical Hematologist/Oncologist Dubuque, Iowa Not Medical Advice or Opinion  

¡Gracias por escuchar! En este episodio se hablará acerca de las alternativas de tratamiento del síndrome de Sjögren primario, tanto glandular como extraglandular.Recuerden que su retroalimentación es bienvenida y les pido amablemente califiquen el podcast en iTunes. Además, Tukua se encuentra disponible en Spotify o a través del gestor de podcasts de su elección.A continuación enlisto algunos de los artículos revisados para este episodio: Vitali, C. et al. Classification criteria for Sjögren’s syndrome: a revised version of the European criteria 21. proposed by the American-European ConsensusGroup. Ann. Rheum. Dis. 61, 554–558 (2002).Shiboski, S. C. et al. American College of 22. Rheumatology classification criteria for Sjögren’ssyndrome: a data-driven, expert consensus approach in the Sjögren’s International Collaborative Clinical 23. Alliance cohort. Arthritis Care Res. (Hoboken) 64, 475–487 (2012).Seror, R. et al. EULAR Sjögren’s syndrome disease activity index: development of a consensus systemic 25. disease activity index for primary Sjögren’s syndrome. Ann. Rheum. Dis. 69, 1103–1109 (2010).Seror, R. et al. Defining disease activity states and clinically meaningful improvement in primary Sjogren’s 26. syndrome with EULAR primary Sjögren’s syndrome disease activity (ESSDAI) and patient-reported indexes (ESSPRI). Ann. Rheum. Dis. 75, 382–389 (2016).Seror, R. et al. EULAR Sjögren’s Syndrome Patient 27. Reported Index (ESSPRI): development of a consensus patient index for primary Sjögren’s syndrome. Ann. Rheum. Dis. 70, 968–972 (2011).Theander, E. et al. Lymphoid organisation in labial salivary gland biopsies is a possible predictor for the 28. development of malignant lymphoma in primary Sjögren’s syndrome. Ann. Rheum. Dis. 70, 29. 1363–1368 (2011).Valim, V. et al. Recommendations for the treatment 33. of Sjögren’s syndrome. Rev. Bras. Reumatol. 55, 446–457 (in Portuguese) (2015).Furness, S., Worthington, H. V., Bryan, G., Birchenough, S. & McMillan, R. Interventions for the management of dry mouth: topical therapies. 34. Cochrane Database Syst. Rev. 12, CD008934 (2011).Steller, M., Chou, L. & Daniels, T. E. Electrical stimulation of salivary flow in patients with Sjögren’s syndrome. J. Dent. Res. 67, 1334–1337 (1988).Vivino, F. B. et al. Pilocarpine tablets for the treatment of dry mouth and dry eye symptoms in patients with Sjögren syndrome: a randomized, placebo-controlled, fixed-dose, multicenter trial. P92-01 Study Group. Arch. Intern. Med. 159, 174–181 (1999).Meijer, J. M. et al. Effectiveness of rituximab treatment in primary Sjögren’s syndrome:a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 62, 960–968 (2010).Forstot, S. L. & Foulks, G. N. Management of Dry Eye (Oxford Univ. Press, 2012).Toda, I., Shinozaki, N. & Tsubota, K. Hydroxypropyl methylcellulose for the treatment of severe dry eye associated with Sjögren’s syndrome. Cornea 15, 120–128 (1996).Marsh, P. & Pflugfelder, S. C. Topical nonpreserved methylprednisolone therapy for keratoconjunctivitis sicca in Sjögren syndrome. Ophthalmology 106, 811–816 (1999).Barber, L. D., Pflugfelder, S. C., Tauber, J. & Foulks, G. N. Phase III safety evaluation of cyclosporine 0.1% ophthalmic emulsion administered twice daily to dry eye disease patients for up to 3 years. Ophthalmology 112, 1790–1794 (2005).Milin, M. et al. Sicca symptoms are associated with similar fatigue, anxiety, depression, and quality-of-life impairments in patients with and without primary Sjögren’s syndrome. Joint Bone Spine http://dx.doi. org/10.1016/j.jbspin.2015.10.005 (2016).van Leeuwen, N. et al. Psychological profiles in patients with Sjögren’s syndrome related to fatigue: a cluster analysis. Rheumatology (Oxford) 54, 776–783 (2015).Segal, B. et al. Prevalence, severity, and predictors of fatigue in subjects with primary Sjögren’s syndrome. Arthritis Rheum. 59, 1780–1787 (2008).Gottenberg, J. E. et al. Effects of hydroxychloroquine on symptomatic improvement in primary Sjögren syndrome: the JOQUER randomized clinical trial. JAMA 312, 249–258 (2014).Hartkamp, A. et al. Effect of dehydroepiandrosterone administration on fatigue, well-being, and functioning in women with primary Sjögren syndrome: a randomised controlled trial. Ann. Rheum. Dis. 67, 91–97 (2008).Theander, E., Horrobin, D. F., Jacobsson, L. T. & Manthorpe, R. Gammalinolenic acid treatment of fatigue associated with primary Sjögren’s syndrome. Scand. J. Rheumatol. 31, 72–79 (2002).Kruize, A. A. et al. Hydroxychloroquine treatment for primary Sjögren’s syndrome: a two year double blind crossover trial. Ann. Rheum. Dis. 52, 360–364 (1993).Sankar, V. et al. Etanercept in Sjögren’s syndrome: a twelve-week randomized, double-blind, placebo- controlled pilot clinical trial. Arthritis Rheum. 50, 2240–2245 (2004).Koch, M., Iro, H. & Zenk, J. Stenosis and other non- sialolithiasis-related obstructions of the major salivary gland ducts. Modern treatment concepts. HNO 58, 218–224 (in German) (2010).De Vita, S. et al. Efficacy and safety of belimumab given for 12 months in primary Sjögren’s syndrome: the BELISS open-label phase II study. Rheumatology (Oxford) (2015). Kuhn, A. et al. Influence of smoking on disease severity and antimalarial therapy in cutaneous lupus erythematosus: analysis of 1002 patients from the EUSCLE database. Br. J. Dermatol. 171, 571–579 (2014).Palm, O. et al. Clinical pulmonary involvement in primary Sjögren’s syndrome: prevalence, quality of life and mortality — a retrospective study based on registry data. Rheumatology (Oxford) 52, 173–179 (2013).Francois, H. & Mariette, X. Renal involvement in primary Sjögren syndrome. Nat. Rev. Nephrol. 12, 82–93 (2016).Evans, R. D., Laing, C. M., Ciurtin, C. & Walsh, S. B. Tubulointerstitial nephritis in primary Sjögren syndrome: clinical manifestations and response to treatment. BMC Musculoskelet. Disord. 17, 2 (2016).Gottenberg, J. E. et al. Efficacy of rituximab in systemic manifestations of primary Sjögren’s syndrome: results in 78 patients of the AutoImmune and Rituximab registry. Ann. Rheum. Dis. 72, 1026–1031 (2013).Colafrancesco, S. et al. Myositis in primary Sjögren’s syndrome: data from a multicentre cohort. Clin. Exp. Rheumatol. 33, 457–464 (2015).Oddis, C. V. et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum. 65, 314–324 (2013).Mok, C. C., Ho, L. Y. & To, C. H. Rituximab for refractory polymyositis: an open-label prospective study. J. Rheumatol. 34, 1864–1868 (2007).Carvajal Alegria, G. et al. Epidemiology of neurological manifestations in Sjögren’s syndrome: data from the French ASSESS Cohort. RMD Open 2, e000179 (2016).Yamashita, H. et al. Diagnosis and treatment of primary Sjögren syndrome-associated peripheral neuropathy: a six-case series. Mod. Rheumatol. 23, 925–933 (2013).Chen, W. H., Yeh, J. H. & Chiu, H. C. Plasmapheresis in the treatment of ataxic sensory neuropathy associated with Sjögren’s syndrome. Eur. Neurol. 45, 270–274 (2001).Mekinian, A. et al. Efficacy of rituximab in primary Sjögren’s syndrome with peripheral nervous system involvement: results from the AIR registry. Ann. Rheum. Dis. 71, 84–87 (2012).Terrier, B. et al. Non HCV-related infectious cryoglobulinemia vasculitis: results from the French nationwide CryoVas survey and systematic review of the literature. J. Autoimmun. 65, 74–81 (2015).Singh, A. G., Singh, S. & Matteson, E. L. Rate, risk factors and causes of mortality in patients with Sjögren’s syndrome: a systematic review and meta- analysis of cohort studies. Rheumatology (Oxford) 55, 450–460 (2016).Pollard, R. P. et al. Treatment of mucosa-associated lymphoid tissue lymphoma in Sjögren’s syndrome: a retrospective clinical study. J. Rheumatol. 38, 2198–2208 (2011).Papageorgiou, A. et al. Predicting the outcome of Sjögren’s syndrome-associated non-hodgkin’s lymphoma patients. PLoS ONE 10, e0116189 (2015).Devauchelle-Pensec, V. et al. Improvement of Sjögren’s syndrome after two infusions of rituximab (anti-CD20). Arthritis Rheum. 57, 310–317 (2007).Carubbi, F. et al. Efficacy and safety of rituximab treatment in early primary Sjögren’s syndrome: a prospective, multi-center, follow-up study. Arthritis Res. Ther. 15, R172 (2013).Devauchelle-Pensec, V. et al. Which and how many patients should be included in randomised controlled trials to demonstrate the efficacy of biologics in primary Sjögren’s syndrome? PLoS ONE 10, e0133907 (2015).Jousse-Joulin, S. et al. Brief report: ultrasonographic assessment of salivary gland response to rituximab in primary Sjögren’s syndrome. Arthritis Rheumatol. 67, 1623–1628 (2015).Cornec, D. et al. Development of the Sögren’s Syndrome Responder Index, a data-driven composite endpoint for assessing treatment efficacy. Rheumatology (Oxford) 54, 1699–1708 (2015).

Antonella Zucchetto, CRO Aviano, Italy speaks on "Flow cytometry for basic research and diagnosis of lymphoid malignancies". This movie is part of "Flow cytometry: from basic principles to advanced application" Course, 8-10 May 2019, ICGEB Trieste, Italy.

Dr Dan Guerra presents "T regulatory Cells in Human Biology and Disease. An update on transcriptional control". Vol.I. This first segment introduces the elaborate nature of innate and acquired lymphoid cells and the transcription factors that drive lineage differentiation. --- Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Dan Littman discusses the opposing roles of Th17 cells. They protect mucosal surfaces from infection with bacteria and fungi, but they can also cause autoimmune inflammation.

Dan Littman discusses the opposing roles of Th17 cells. They protect mucosal surfaces from infection with bacteria and fungi, but they can also cause autoimmune inflammation.

The doctors of awesome solve the case of the Woman Who Visited Lebanon, and reveal that immunoglobulins protect the olfactory organ of trout against infection with the Ich parasite. Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiP. Links for this episode: Mucosal Ig protect trout from Ich (PLoS Path) Hero: Sir Patrick Manson Letters read on TWiP 163 Case Study for TWiP 163 From here in US before leaving for Uganda: male has lesion affecting nose. Has been having problem with nose for 2 yr, in 40s, surfer, hit nose with board. Southern eastern Costa Rica. After that had blood and scabs from nose. Inside of nares, scab formed. Did not improve with time. Saw ENT doc on LI, said he hit nose and needs reconstructive surgery. Entire septum destroyed. 20+ years ago had non healing ulcer on left hand, saw physician in CR, was treated for 20 days. Send your case diagnosis, questions and comments to twip@microbe.tv Music by Ronald Jenkees

The TWiVerati discuss the FDA Advisory Committee deliberation on the anti-poxvirus drug tecovirimat, and immune cells in gut-associated lymphoid tissue as the major target during acute murine norovirus infection. Hosts: Vincent Racaniello, Dickson Despommier, Alan Dove, Rich Condit, and Kathy Spindler Become a patron of TWiV! Links for this episode ASM Microbe 2018 Support Viruses & Cells Gordon Conference Faculty positions at Icahn School of Medicine FDA meeting materials for tecovirimat(FDA) SIGA Briefing Information (pdf) Errata to the SIGA Briefing Information (pdf) Gut immune cells major targets of norovirus infection(Nat Micro) RNAscope(J Mol Diag) Image credit Letters readon TWiV 493 Weekly Science Picks Alan - Personal Finance for PhDsby Emily Roberts Kathy- Optical illusions fool artificial intelligence Rich- 2017-2018 snowfall graphic Dickson- Dust from the Sahara Vincent - The Last Days of Smallpoxby Mark Pallen Listener Pick Intro music is by Ronald Jenkees. Send your virology questions and comments to twiv@microbe.tv

Dr Aaron Logan speaks with ecancertv at AACR 2016 about developments in determining the levels of residual disease presence in patients following treatment. He reports that, utilising the molecular techniques becoming available, detecting the signs of a patient's deep disease response are an effective predictor of disease free survival. With novel technologies becoming standardised techniques, the ability to determine a patients cancer clonotype and search for its remission in greater detail than light microscopy alone may make it possible to improve screening, therapy, and response duration.

Dr. Krem discusses age-related and biological factors for low-grade lymphoma pathogenesis and outcomes. He then explains the mechanisms of action from low-grade lymphoma therapies.  He finishes by applying recent efficacy and toxicity data to older patients with low-grade lymphoma.   Some items in this lecture may have come from the lecturer’s personal academic files or have been cited in-line or at the end of the lecture. For more information, see our citation page. Disclaimers ©2015 LouisvilleLectures.org

Rachel Golub and Eric Vivier discuss signaling events that control the plasticity of Group 3 innate lymohoid cells.

Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin The TWiPtastic trio solves the case of the Surfer from Switzerland, and reveal how taste-chemosensory tuft cells in the gut regulate immune responses to parasites. Links for this episode: Taste-chemosensory cells and parasite gut immunity (Science) Image credit Letters read on TWiP 107 This episode is sponsored by ASM Agar Art Contest and ASM Microbe 2016  Case study for TWiP 107 Todays case is a fun case about a 45 year old gentleman from Assam India, with sixteen years of fever, abdominal pain, darkening of skin, yellowing of eyes. Farmer, does not have much energy. Works barefoot in fields. Fever occurs every other day. Prior medical problems, nothing out of the ordinary. No surgeries, no meds, has never seen physician. Married, kids, no extramarital affairs, HIV negative, eats mostly cooked vegetables. Lives in concrete house, no screens, mosquito netting. Other people in area have similar problems. Water comes from pump, fill plastic jugs. Been in Assam sick his whole life, finally came to regional med center for evaluation. Underweight. No pets. Dogs around, avoids dogs. Cows, monkeys are around. Fair appetite. Exam: febrile, in face can see darkening which is increasing, also extremities. Whites of eyes are yellow (jaundiced). Striking is has a very large liver, spleen. Elevated bilirubin. Some increased liver enzymes. No physical scarring or lesions. Send your diagnosis to twip@microbe.tv Send your questions and comments to twip@microbe.tv

Lymphoid and non-lymphoid tissues accommodate defined numbers of dendritic cells (DCs). There, DC-life span is influenced by various components such as proliferation and cell division triggered by cytokines, maturation processes in response to extracellular inflammatory and microbial substances, as well as induction of migration and apoptosis. Previous work has demonstrated the importance of specific numbers of DCs in tissues, as changes of DC numbers or DC life span could alter immunity, tolerance or inflammation resulting in various immune diseases. However, currently it is still unknown how DC life span and homeostasis is regulated in vivo. RhoA is a member of Rho GTPase-family, which plays important roles in regulating cytoskeleton organization, proliferation, migration and survival. However, our current knowledge about RhoA-functions is based mostly on studies using dominant negative and constitutively active RhoA-mutants, which have possible unspecific effects on other members of the Rho GTPase family. Therefore, we used a LoxP/Cre recombinase approach to knock out RhoA selectively in DCs. Here we found that GTPase RhoA controlled the homeostasis of mature DCs, and deletion of RhoA caused significantly reduced numbers of CD8+CD11b- and CD11b+Esamhi DC subsets, while CD11b+Esamlo DCs remained largely unaltered. Loss of RhoA interfered with homeostatic proliferation, cytokinesis, survival and turnover of cDCs. By performing proteomic analysis, we found that a pro-survival PI3Kγ/Akt/BAD pathway was deregulated in RhoA-ko DCs. Taken together, our findings indicate that RhoA plays a critical role in regulating DC-homeostasis, deletion of which decreases DC numbers resulting in impaired immune protection.

Tanya M. Wildes, MD, MSCI, Washington University School of Medicine, discusses the treatment options for lymphoid malignancies in the older patient.

Dr Strasser talks to ecancertv at ASH 2013. Impaired apoptosis is considered one of the prerequisites for the development of most, if not all, cancers, but the mechanisms that guarantee the sustained survival of most cancer cells remain unknown. Members of the Bcl-2 family are key regulators of apoptosis and include proteins essential for cell survival and those required to initiate cell death. Studies with transgenic mice have shown that over-expression of Bcl-2 or related pro-survival family proteins, such as Bcl-xL or Mcl-1, can promote tumorigenesis, particularly in conjunction with mutations that deregulate cell cycle control, such as deregulated c-myc expression. It is, however, not known whether expression of pro-survival Bcl-2 family members under endogenous control is required to maintain the survival of cells undergoing neoplastic transformation. Using Eµ-myc transgenic mice, a well-characterized model of human Burkitt’s lymphoma, we investigated the role of endogenous Bcl-2 in lymphoma development. Bcl-2 was found to be dispensable for the development of Eµ-myc pre-B/B lymphoma. In contrast, loss of Bcl-xL and even, more remarkable, loss of a single allele of Mcl1 greatly impaired lymphoma development. Experiments with inducible knockout mice demonstrated that Mcl-1 but not Bcl-xL is essential for the sustained survival and expansion of Myc-driven malignant pore-B/B lymphoma. Remarkably, even loss of one Mcl1allele greatly impaired lymphoma growth. These findings were translated into using lymphoid malignancies by using inducible expression of selective antagonists of distinct pro-survival Bcl-2 family members. Such studies showed that Mcl-1 is also critical for the sustained survival and expansion of Burkitt Lymphoma, a Myc-driven malignancy. These observations indicate that (even relatively weak) targeting of Mcl-1 may be an attractive strategy.

Dr Partow Kebriaei talks to ecancer at the 18th EHA Congress about her abstract on artificial antigen presenting cells that generate T cells expressing CD19-specific chimeric antigen receptor in order to prevent relapse in lymphoid malignancies.

Interview with Prof. Ronald McCaffrey, Hemato-Oncologist af Brigham&Womens hospital and Harward Medical School. Prof McCaffrey talks about Terminal deoxynucleotidyl transferase (tDT) as a therapeutic target in lymphoid malignancies. The interview is led by Shaun McCann, Chair of EHATol Unit, Member of EHA Education Committee.

Interview with Prof. Ronald McCaffrey, Hemato-Oncologist af Brigham&Womens hospital and Harward Medical School. Prof McCaffrey talks about Terminal deoxynucleotidyl transferase (tDT) as a therapeutic target in lymphoid malignancies. The interview is led by Shaun McCann, Chair of EHATol Unit, Member of EHA Education Committee.

Wed, 28 Nov 2007 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/7762/ https://edoc.ub.uni-muenchen.de/7762/1/Petropoulos_Konstantin.pdf Petropoulos, Konstantin

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Sat, 1 Jan 1994 12:00:00 +0100 https://epub.ub.uni-muenchen.de/6911/1/6911.pdf Bensinger, W.; Singer, J.; Storb, R.; Rowley, S.; Longin, K.; Appelbau, F. R.; Lilleby, K.; Buckner, C. D.; Weaver, C.; Langenmayer, Irmgard

The distribution of the functional subsets of porcine T cells, the cytolytic/suppressor (Tc/s) and the helper/inducer (Th/i) cells was studied in cryostat sections of thymus, lymph nodes, tonsils, Peyer's patches, spleen and liver using the indirect immunoperoxidase technique. Three murine monoclonal antibodies (mAb) were used. The mAb 8/1 reacts with an antigen present on all T cells and on cells of the myeloid lineage; the antigen has not yet been characterized biochemically. The mAb 295/33 (anti-T8) binds to the porcine T8 antigen and defines the Tc/s subset, while mAb PT-4 (anti-T4) detects the porcine T4 antigen and defines the Th/i subset. Practically all thymocytes were stained by mAb 8/1. The majority of cortical thymocytes apparently co-expressed T8 and T4, whereas distinct fractions of medullary cells were labelled by either anti-T8 or anti-T4. In peripheral lymphoid organs all three mAb reacted with cells in the thymus-dependent areas and with cells scattered in the lymphoid follicles. In lymph nodes, tonsils and Peyer's patches, anti-T8 and anti-T4 each labelled approximately half of the cells stained by mAb 8/1. In the periarteriolar lymphoid sheath of the spleen, anti-T4 labelled more cells than did anti-T8. The reactivity of mAb 8/1 with the Kupffer cells of the liver demonstrated the expression of the 8/1 antigen on cells of the monocyte lineage. The T8 and T4 antigens could not be detected in acetone-fixed and paraffin-embedded sections, while the antigen recognized by mAb 8/1 remained preserved. Altogether, despite an inverted microanatomical structure of porcine lymph nodes, the frequency and distribution of T8+ and T4+ cells in thymus-dependent areas proved to be similar to those found in other species.